Cerebral Blood Flow Responses to Trigeminal Olfactory Stimulation and Their Nicotinic Cholinergic Regulation in Anesthetized Rats.

Information about the sense of smell is conveyed by the olfactory nerve, or by the trigeminal nerve when irritating odors. We recently reported that olfactory nerve stimulation increases regional cerebral blood flow (BF) in the olfactory bulb, and the activation of nicotinic receptors in the brain potentiates olfactory bulb BF responses in anesthetized rats. This study aimed to elucidate the effects of intranasal trigeminal nerve stimulation on regional cerebral BF compared to the olfactory nerves, as well as the impact of nicotinic receptor activation on these BF responses. Regional BF in the olfactory bulb and frontal cortex was measured by laser Doppler flowmeter or laser speckle contrast imager in anesthetized and artificially ventilated rats. Electrical stimulation of the intranasal trigeminal nerve (0.5 ms, 5 mA, 20 Hz, and 5 s) produced a small increase in olfactory bulb BF and robust increases in both frontal cortical BF and arterial pressure. Transecting the upper thoracic spinal cord eliminated the pressor response, and although intranasal electrical stimulation did not elevate the olfactory bulb BF, it increased BF in the frontal cortex. Intravenous injection of nicotine (30 μg/kg), a nicotinic receptor agonist, did not influence the olfactory bulb BF but augmented increased BF in the frontal cortex following the intranasal trigeminal nerve stimulation. In conclusion, this study showed that the intranasal trigeminal nerve stimulation increased BF in the frontal cortex, but not in the olfactory bulb, independent of blood pressure changes. Furthermore, activation of nicotinic cholinergic transmission potentiated the frontal cortical BF responses to intranasal trigeminal stimulation.